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Inhibition by the Landschütz ascites carcinoma of the granulomatous inflammatory response to C. parvum.
I.p. or i.v. administration of Corynebacterium parvum (CP) to MF1 mice induces a generalized inflammatory response, associated with marked hepatosplenomegaly and accompanied by a pronounced granulomatous response in the liver. Injection of the Landschütz ascites carcinoma (LAC) 24 h after CP substan...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
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Nature Publishing Group
1982
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2010992/ https://www.ncbi.nlm.nih.gov/pubmed/7073950 |
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author | McIntosh, L. C. Pugh-Humphreys, R. G. Fraser, R. A. Thomson, A. W. |
author_facet | McIntosh, L. C. Pugh-Humphreys, R. G. Fraser, R. A. Thomson, A. W. |
author_sort | McIntosh, L. C. |
collection | PubMed |
description | I.p. or i.v. administration of Corynebacterium parvum (CP) to MF1 mice induces a generalized inflammatory response, associated with marked hepatosplenomegaly and accompanied by a pronounced granulomatous response in the liver. Injection of the Landschütz ascites carcinoma (LAC) 24 h after CP substantially reduced the intensity of the inflammatory response, and decreased both the frequency and size of the hepatic granulomas, as revealed by morphometric analysis of histological sections. The difference in cellular composition of the granulomas between the experimental groups, as revealed by light microscopy, was further emphasized and characterized by ultrastructural studies. These revealed the predominance of macrophages within the granulomas in tumour-bearing mice, in contrast to the predominance of epithelioid cells in the lesions which developed in mice given CP alone. Our experimental findings show that the inhibitory effect of the growing LAC on granuloma formation in response to CP cannot be ascribed to (a) sequestration of the microorganism within the growing tumour, (b) a nonspecific inflammatory stimulus, (c) diversion and seqestration of mononuclear phagocytes in the growing tumour or (d) the presence of lactate dehydrogenase-elevating virus in either the host or tumour cells. The inhibition of liver granuloma formation is consistent with an effect mediated by soluble, heat-stable tumour-associated factor(s). IMAGES: |
format | Text |
id | pubmed-2010992 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1982 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-20109922009-09-10 Inhibition by the Landschütz ascites carcinoma of the granulomatous inflammatory response to C. parvum. McIntosh, L. C. Pugh-Humphreys, R. G. Fraser, R. A. Thomson, A. W. Br J Cancer Research Article I.p. or i.v. administration of Corynebacterium parvum (CP) to MF1 mice induces a generalized inflammatory response, associated with marked hepatosplenomegaly and accompanied by a pronounced granulomatous response in the liver. Injection of the Landschütz ascites carcinoma (LAC) 24 h after CP substantially reduced the intensity of the inflammatory response, and decreased both the frequency and size of the hepatic granulomas, as revealed by morphometric analysis of histological sections. The difference in cellular composition of the granulomas between the experimental groups, as revealed by light microscopy, was further emphasized and characterized by ultrastructural studies. These revealed the predominance of macrophages within the granulomas in tumour-bearing mice, in contrast to the predominance of epithelioid cells in the lesions which developed in mice given CP alone. Our experimental findings show that the inhibitory effect of the growing LAC on granuloma formation in response to CP cannot be ascribed to (a) sequestration of the microorganism within the growing tumour, (b) a nonspecific inflammatory stimulus, (c) diversion and seqestration of mononuclear phagocytes in the growing tumour or (d) the presence of lactate dehydrogenase-elevating virus in either the host or tumour cells. The inhibition of liver granuloma formation is consistent with an effect mediated by soluble, heat-stable tumour-associated factor(s). IMAGES: Nature Publishing Group 1982-04 /pmc/articles/PMC2010992/ /pubmed/7073950 Text en https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Research Article McIntosh, L. C. Pugh-Humphreys, R. G. Fraser, R. A. Thomson, A. W. Inhibition by the Landschütz ascites carcinoma of the granulomatous inflammatory response to C. parvum. |
title | Inhibition by the Landschütz ascites carcinoma of the granulomatous inflammatory response to C. parvum. |
title_full | Inhibition by the Landschütz ascites carcinoma of the granulomatous inflammatory response to C. parvum. |
title_fullStr | Inhibition by the Landschütz ascites carcinoma of the granulomatous inflammatory response to C. parvum. |
title_full_unstemmed | Inhibition by the Landschütz ascites carcinoma of the granulomatous inflammatory response to C. parvum. |
title_short | Inhibition by the Landschütz ascites carcinoma of the granulomatous inflammatory response to C. parvum. |
title_sort | inhibition by the landschütz ascites carcinoma of the granulomatous inflammatory response to c. parvum. |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2010992/ https://www.ncbi.nlm.nih.gov/pubmed/7073950 |
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